Separating the DNA within Gamete Cells.

I have an observation and a question. How do male and female gamete cells divide their genes so there is minimal genetic redundancy within the offspring?

For example, if I could clone a male and female, from one of their cells, each has the DNA needed to make, 2 eyes, 1 nose, 2 arms, etc. If we next look at their gamete cells, the DNA divides in half, but needs to do so in a way that will not result in 4 eyes, 2 noses or 4 arms within the offspring. The division of the DNA needs to be ordered for both the male and female, so we end up with only one set of genes for each of the above. We can end up with our mothers nose and father eyes, but not both our mother and fathers eyes (4).

I can sort of see how the female gamete cells might do this since they extrude the extra DNA. But with male sperm cells, all the DNA is used. Does this means that half the sperm cannot merge, by default, via some membrane screening mechanism? If sperm attachment was random why not four eyes half the time?

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We are diploid. Each of our 23 chromosomes are paired, one from from each parent. Gametes are produced by meiosis, which randomly combines mother and father DNA by the process of crossover:

There is no redundancy, just a lateral shift of randomly crossed segments. This is nature's way of randomly shuffling the traits between the parents at the moment the gamete forms. But the gamete is haploid, having only 23 single but interspliced chromosomes.

In fertilization, gametes join, to form the zygote which will incorporate DNA from both parents.

The zygote will split for many generations, then cleave into a spherical blastula, from which will develop the body. The zygote has 23 pairs of of chromosomes.

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Normal cells in your body are diploid cells, containing 23 pairs of chromosomes. Each chromosome is a long strand of DNA.
Most of the paired DNA is the same. Areas where a chromosome is (potentially) different from its partner are called alleles.

Loosely speaking, the DNA that makes things that are the same for all humans (2 eyes, 1 nose, 2 arms, etc) are in the bits where the two halves of the pair are the same.
The things that are different between different people are in the alleles.

Now.

Sperm and ova are are haploid cells, containing 23 single chromosomes.
Haploid cells are made in a process called Meiosis:

When a sperm fertilizes an ovum, the chromosomes pair up to make a diploid cell.

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For example, if I could clone a male and female, from one of their cells, each has the DNA needed to make, 2 eyes, 1 nose, 2 arms, etc. If we next look at their gamete cells, the DNA divides in half, but needs to do so in a way that will not result in 4 eyes, 2 noses or 4 arms within the offspring. The division of the DNA needs to be ordered for both the male and female, so we end up with only one set of genes for each of the above. We can end up with our mothers nose and father eyes, but not both our mother and fathers eyes (4).

I can sort of see how the female gamete cells might do this since they extrude the extra DNA. But with male sperm cells, all the DNA is used. Does this means that half the sperm cannot merge, by default, via some membrane screening mechanism? If sperm attachment was random why not four eyes half the time?

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O….M…..G…….

So, let me get this right. You spam the B&G subforum with endless pronouncements and lectures about how life and cells and DNA and evolution works (which I have mostly moved here for collective evidence), and here you demonstrate that you don’t even understand some of the most basic genetic concepts, namely diploidy and meiosis.

I think it’s time to start treating you like a full on pseudoscience troll that you are.

I can sort of see how the female gamete cells might do this since they extrude the extra DNA. But with male sperm cells, all the DNA is used.

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Are you thinking about the polar bodies that are formed during oogenesis, as an oocyte develops into an ovum?

That's meiosis, which also happens in spermatogenesis.

The difference is that each spermatocyte makes four separate spermatids during meiosis, while an oocyte only makes one ovum, while the other three cells become polar bodies (if I remember rightly they kind of hang around in the ovum for a while and are eventually broken down.)

Corrections welcome.
I'm reasonably pleased with how much of this I remember, considering it was crammed in to the repro module around lots of pathology, anatomy, psychosocial stuff, and all the other repro physiology and I never studied biology before... but I do love Wikipedia for the quick confirmation and vocabulary reminder.

I think it’s time to start treating you like a full on pseudoscience troll that you are.

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HR, it appears that the others are still giving him a chance to learn, notwithstanding his trolling.

In that vein, it should be mentioned that in many organisms (land plants, sea algae, etc.) the adult phase is haploid, from which are produced haploid sex cells which then fuse to form a diploid zygote which then immediately undergoes meiosis, forming cells that grow into the adult form as haploid. In some species, the adult form can be either the haploid or the diploid.

This is also true for some animals, such as bees, wasps and ants which develop from unfertilized haploid eggs, are therefore haploid in their adult form.

DNA from the Beginning is one of the best genetics tutorials I have found. It provides a comprehensive coverage of classical and molecular genetics using graphics and animations.

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I like that link you gave. The presentation format is very good about removing information clutter and not too many clicks to access any page. I also like the biographies, to help remind us how this knowledge was uncovered.

This is an excellent chance for wellwisher (and any other person who had problems with evolution) to recognize how truly random mutations can be. Once you accept that the chromatids naturally exchange DNA, and how truly random that process is, it takes only a little contemplation to recognize that other "unintended" kinds of DNA alteration can also randomly occur.

(I mention this since the notion of randomness seems to clash with the fundamentalist doctrine of determinism.)

I was more concerned with how does an integrated animal or human form, without redundancy in some of its many bulk systems (eyes, nose, liver, etc.) using a random separation and recombination of genes? If there are both male and female genes for eyes, how does it only pick one and not both or one of each?

I could always follow what was presented, but this does not answer all the questions. in terms of the final integration of a lifeform from a combination of random and redundant genes. Some method of order would make more sense.

As an analogy we have two puzzles. We split each puzzle into two and then merge the two halves to get a third. If you try to built this composite puzzle, the puzzle will be incomplete the vast majority of the time.

I was more concerned with how does an integrated animal or human form, without redundancy in some of its many bulk systems (eyes, nose, liver, etc.) using a random separation and recombination of genes? If there are both male and female genes for eyes, how does it only pick one and not both or one of each?

I could always follow what was presented, but this does not answer all the questions. in terms of the final integration of a lifeform from a combination of random and redundant genes. Some method of order would make more sense.

As an analogy we have two puzzles. We split each puzzle into two and then merge the two halves to get a third. If you try to built this composite puzzle, the puzzle will be incomplete the vast majority of the time.

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Just use what you always use when you don't understand something - it is due to entropy.

If there are both male and female genes for eyes, how does it only pick one and not both or one of each?

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Your question is very confused; I can’t understand what you’re asking. Are you asking how does a diploid offspring inherit one paternal and one maternal allele for each gene? The answer is meiosis – use the above links to clarify this process.

Or, are you asking how does a given cell know which allele of a given gene to use? The answer is that for the significant majority of traits both alleles (the paternal and maternal alleles) of a given gene contribute to the trait.

As an analogy we have two puzzles. We split each puzzle into two and then merge the two halves to get a third. If you try to built this composite puzzle, the puzzle will be incomplete the vast majority of the time.

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That’s an inaccurate analogy for the transmission of alleles from parents to offspring. Again, an understanding of the process of meiosis (and chromosomes, and alleles, and sister chromatids, and DNA replication) would clear this up. Contrary to what you have said, following the above links will answer all the questions.

I was more concerned with how does an integrated animal or human form, without redundancy in some of its many bulk systems (eyes, nose, liver, etc.) using a random separation and recombination of genes? If there are both male and female genes for eyes, how does it only pick one and not both or one of each?

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There are a few answers to your question:

1) There's no such thing as "male and female genes for eyes." The alleles that code for your eyes are spread across your genome.

2) Male and female genomes are different only in one pair of chromosomes, the familiar XX and XY chromosome pairs. ("XY" denotes one standard looking chromosome and one truncated chromosome.) The SRY gene (sex-determining region of the Y chromosome) is what makes males males. This doesn't always work, and thus you can have a phenotypic female with an XY genome.

3) Rarely is there a geographic mapping for any trait i.e. "gene HOX21A codes for your left eye." There are hundreds if not thousands of genes that code for eye development. For example, one set of genes creates the ectoderm germ layer during very early development; another set causes a portion of that layer to thicken and produce a cornea from that layer.

I could always follow what was presented, but this does not answer all the questions. in terms of the final integration of a lifeform from a combination of random and redundant genes. Some method of order would make more sense.

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There is a method of order; research the HOX gene complex, for example.

However there are a tremendous number of genes that go into every structure, with a lot of redundancy. You can remove a single gene and often its partner on the other chromosome will take over for it. You can remove both and 99% of the time other genes will compensate. You have to hammer a genome pretty hard (like put an entire extra chromosome into the genome, or take an entire one out) before you see serious problems - and even then, sometimes the human it codes for survives, albeit with serious deficits.

As an analogy we have two puzzles. We split each puzzle into two and then merge the two halves to get a third. If you try to built this composite puzzle, the puzzle will be incomplete the vast majority of the time.

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Ah, but the genome is not like a puzzle. It's more like a hologram. Take away a little of the hologram and you still have the complete image. Take away a little more and it gets more grainy - but it's still all there. Mix two holograms any way you like and you'll get a superposition of two images, one on top of the other.

Your analysis suggests the entire DNA, is like a team, which is more than the sum of its parts. If we remove genes, other genes can compensate, because the team still adds up to more than the sum of the parts minus one.

Or, are you asking how does a given cell know which allele of a given gene to use? The answer is that for the significant majority of traits both alleles (the paternal and maternal alleles) of a given gene contribute to the trait.

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That's probably it. What he needs to learn about is Dominant versus Recessive genes. Mutations usually create a deleterious recessive (if passed down through the generations, and subsequently inherited from both parents, results in a deleterious situation, usually fatal; if only one inherited, then the other comparable gene (allele) from the other parent becomes the only functioning one (Dominant).

Your analysis suggests the entire DNA, is like a team, which is more than the sum of its parts. If we remove genes, other genes can compensate . . . .

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In many cases yes. The most common case of this is homozygousity (now there's a word of the day.) That's the case where we have two alleles for a trait, one on each paired chromosome. This is also one of the keys to standard Mendelian genetic inheritance.

For example, let's say you have an important set of genes that codes for red blood cell shape. Normally you have two of these, one on each chromosome. In some cases one might be defective. You might expect that would result in malformed red blood cells, but the intact genetic information on the other chromosome compensates for it.

Thus you can be heterozygous for sickle cell anemia (i.e. be missing the correct genes on one chromosome) but never notice anything wrong. It's only if _both_ chromosomes are damaged that you notice anything wrong.

And even then it's not instantly fatal. Even before medical care people sometimes lived to age 20 or so, and nowadays people with sickle cell anemia can live to age 50 or 60. That's because there are enough "backups" in our biology to compensate for the distorted shape and impaired function of the malformed red blood cells characteristic of sickle cell anemia.

Your analysis suggests the entire DNA, is like a team, which is more than the sum of its parts. If we remove genes, other genes can compensate, because the team still adds up to more than the sum of the parts minus one.

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In order to understand how organs arise from the zygote, you need to understand cell differentiation. Remember, the zygote starts as a single celled creature having all of he DNA to produce the multi-cellular creature. How does that happen? How do some cells become bone, others feathers, etc., when they all carry the same DNA?

Here is an illustration of the development from zygot to blastocyst, which is where the embryonic stem cells are born:

What I see are chemical gradients, such as in the early blastocyst stage. The morula stage is symmetrical and lacks a gradient. This might be as far as it can go. It needs a potential to set a gradient before it can go any farther.

In the human body, the primary chemical gradient appears to be between the nervous system and the blood supply. This is inferred from the exterior membrane potential of neurons with is positive/maximized, and the blood supply which is slightly alkaline or slight negative charge. The ratio of these (net potential in the context of ratio and quantity) helps maintain differentiation.

As long as the gradients are not damaged the configurational equilibria (team shape) associated with the DNA can develop normally. The configurational equilibria on the DNA (team shape) made easier by the way chromosomes are organized. These are also in the form of gradients. This is inferred based on aspects of the DNA remaining packed, while unpacking depends on chemical equilibrium.

We have an external gradient imposing external potentials, which impact the potential gradient at the membrane (membrane potential), which impacts the genetic gradient. This allows the genetic teams to be more than the sum of its parts. If we lose one gene the equilibrium DNA configuration redistributes in 3-D.

What I see are chemical gradients, such as in the early blastocyst stage. The morula stage is symmetrical and lacks a gradient. This might be as far as it can go. It needs a potential to set a gradient before it can go any farther.

In the human body, the primary chemical gradient appears to be between the nervous system and the blood supply. This is inferred from the exterior membrane potential of neurons with is positive/maximized, and the blood supply which is slightly alkaline or slight negative charge. The ratio of these (net potential in the context of ratio and quantity) helps maintain differentiation.

As long as the gradients are not damaged the configurational equilibria (team shape) associated with the DNA can develop normally. The configurational equilibria on the DNA (team shape) made easier by the way chromosomes are organized. These are also in the form of gradients. This is inferred based on aspects of the DNA remaining packed, while unpacking depends on chemical equilibrium.

We have an external gradient imposing external potentials, which impact the potential gradient at the membrane (membrane potential), which impacts the genetic gradient. This allows the genetic teams to be more than the sum of its parts. If we lose one gene the equilibrium DNA configuration redistributes in 3-D.

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Keep in mind the gradient shown was inside the embryo, not an external influence. And this is not a chemical gradient per se, but a variation on the concentration of proteins that will turn on transcription factors inside the stem cells, to promote further differentiation. What you are seeing is programmed mutations taking place in a way that fast-forwards through the countless stages of evolution, yet implemented by forcing the transcription factors to unzip and express particular genes, even if these are only needed to build the banded regions where future generations of stem cells will "evolve".

The clip shows how nature exploits chemistry in ways that defy simplification, or the imposition of "reasoned" design. The complexity is traced to stages of development, from the earliest of notochords (flatworms) to vertebrate marine animals, amphibians, reptiles, birds, and tetrapods, which bridged the evolution from reptilian to mammalian forms.

Each stage of evolution introduces "tweaks" but preserves huge inherited chunks of chemical processing layers in embryonic development. This gives further incontrovertible proof that "design" is by natural selection, nothing more, as the refinements seen in embryogenesis encapsulate the successes of prior life forms, retain them, and reuse them simply because they work and are handed down genetically.

As you see, once life forms were able to produce one "stripe" by this method, nature has arrived at 14 stripes by the time we get to the mosquito. And each of those stripes becomes a zone for further specialization to a body part, so if zone 10 were to represent the shoulder area, that is where the appendage for the front legs will further develop, from a bud.

The human embryo follows the exact game plan. As mentioned by billvon above, a thousand genes may be involved in the development of a particular organ. A particular gene has such a specific purpose, that the overall effect, to produce a particular organ or tissue, is only possible because hundreds or thousands of these interactions are carried out in sequence upon sequence, until each of the 200 or so different cell types (in the human body) are completely and finally differentiated out of the stem cells that work their magic during early development.

We talked about the development from zygote to blastocyst, which is the hollow sphere, and you saw the genesis of the embryonic mass, where the stem cells arise in the banded regions. What I would like to show you next is what happens as the embryo first starts budding and amassing primitive structures that are localized to each band, and yet able to maintain a connection, like a string of pearls, so the body plan remains continuous, yet able to differentiate locally.

This next clip begins where we left off, only here we see the early embryo from outside, as the striped zones begin to specialize further. You will see a flat substrate, which is the embryo itself. This shape proves we evolved from reptiles, because they needed more yolk to survive egg deployment on dry land. The space needed by the yolk required a flat embryo. Mammals don't require a yolk, but we inherited the flat structure, because nature had already designed it, and nature doesn't fix what aint broke. From this flat embryo a "primitive streak" develops. This is inherited from worms. The notochord they possess appears out of the streak, and will form two ridges. What happens next is a folding and curling that was worked out in early vertebrates to form the spinal tube and neural crest from which the vertebrae, spinal chord and brain will bud and develop. What you see playing out is a reenactment of evolution, in stage upon stage of formation and refinements added by mutation upon mutation. Yet these stages are stitched together seamlessly, so the transitions of 400 million years pass before your eyes in moments, or in a few weeks in the life of a human embryo. Notice that the embryonic disk differentiates into germ layers (ectoderm, endoderm, mesoderm) that each follow their own specialized tracks of development in this process, which is called gastrulation: